C1-esterase inhibitor prevents early pulmonary dysfunction after lung transplantation in the dog
| Autor: | Rosario Lopez-Pedrera, J. Lopez-Pujol, F. López-Rubio, Rafael Guerrero, Francisco Velasco, Mariano Rodriguez, A Alvarez, J Carracedo, Ramírez R, Angel Salvatierra |
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| Rok vydání: | 1997 |
| Předmět: |
Lung Diseases
Pulmonary and Respiratory Medicine Pathology medicine.medical_specialty medicine.medical_treatment Leukocyte adhesion molecule Ischemia Complement C1 Inactivator Proteins Critical Care and Intensive Care Medicine Hypoxemia Dogs Postoperative Complications medicine Animals Lung transplantation Hypoxia Lung Pulmonary Gas Exchange business.industry Respiratory disease Hemodynamics respiratory system medicine.disease respiratory tract diseases Transplantation Disease Models Animal medicine.anatomical_structure Reperfusion Injury medicine.symptom business Reperfusion injury Lung Transplantation |
| Zdroj: | ResearcherID |
| ISSN: | 1535-4970 1073-449X |
| Popis: | The success of lung transplantation to a large extent depends on effective protection of the graft from ischemic injury after reperfusion. Although mechanisms have not been clarified, the pathologic findings of ischemic injury after reperfusion are similar to adult respiratory distress syndrome, a condition in which the blood coagulation contact system is activated. This study evaluates the effect of C1-esterase inhibitor (C1-INH), the main inhibitor of the blood coagulation contact system, on short-term lung function in a dog model of orthotopic lung transplantation. Twelve lung transplantations were performed after 24 h of ischemic time. Dogs were randomly assigned to receive either vehicle (Control) or C1-INH. After the lung transplantation in the control group, Pao2 decreased by 84% and both the AaPO2 and the Qs/Qt% increased (340 and 530%, respectively, p < 0.01); these parameters remained unchanged in the C1-INH group. The hypoxemia observed in control animals was associated with decreased blood coagulation contact factors, complement consumption, increased expression of adhesion glycoproteins in leukocytes, and extensive intraalveolar and interstitial neutrophil infiltration. In contrast, C1-INH administration prevented hypoxemia, the decrease in blood coagulation contact factors, the activation of the complement system, the increase in expression of leukocyte adhesion molecules, and inflammatory cell infiltrate. This study has demonstrated that in a dog model of lung transplantation, the administration of C1-INH prevents early pulmonary dysfunction, and it suggests that activation of blood coagulation contact system and complement are important mechanisms causing ischemic injury after reperfusion. |
| Databáze: | OpenAIRE |
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